Effect of carbohydrate feeding on insulin action in skeletal muscle after surgical trauma in the rat☆
Accepted 25 October 2000.
Abstract
Metabolic stress after surgery is associated with peripheral insulin resistance. Recent studies have suggested that preoperative glucose can ameliorate postoperative decreases in insulin-stimulated glucose disposal. In the present experiments, we used a bowel-resection model of surgical trauma to test the hypothesis that elevations of serum insulin induced by preoperative oral glucose or ad libitum feeding affects postoperative insulin-stimulated glucose uptake in skeletal muscle. Insulin-stimulated glucose transport was measured in vitro in soleus muscles after surgical trauma in fasted rats given oral glucose or water before surgery. Insulin-stimulated glucose transport was also assessed in vitro in fasted or fed traumatized rats and non-traumatized control animals. In addition, stress hormones (glucagon, corticosterone, and adrenaline) were measured before and after surgical trauma in fasted rats and rats fed ad libitum. In vitro skeletal-muscle insulin sensitivity and responsiveness were reduced postoperatively in fasted animals that received oral glucose loads before bowel resections and in rats fed ad libitum or fasted before surgery versus non-traumatized rats (all P < 0.05). Stress-hormone concentrations after trauma did not differ between fed and fasted animals. In the current study, insulin sensitivity and responsiveness were reduced in isolated skeletal muscles after bowel resection, but neither preoperative glucose supplementation nor free intake of mixed nutrients ameliorated the development of postoperative insulin resistance.
aArvid Wretlinds Laboratory for Metabolic and Nutritional Research, Department of Surgery, Karolinska Institute at Huddinge University Hospital, Stockholm, Sweden
bDepartment of Endocrinology, Karolinska Hospital, Stockholm, Sweden
cDepartment of Biology, Adams State College, Alamosa, Colorado, USA
Correspondence to: Lisa Strömmer, MD, Department of Surgery, Huddinge University Hospital, 141 86 Stockholm, Sweden.
☆ This study was supported by grants 00034 and K99-72X-1265-02B from the Swedish Medical Research Council, the Swedish Diabetes Association, and Förenade Liv Mutual Group Life Insurance Company, Stockholm, Sweden.